Intracerebral hemorrhage (ICH) accounts for 10-15% of all strokes and is associated with high mortality and morbidity. Despite significant advances in animal models and understanding of brain injury mechanisms, there is no successful Phase III clinical trial for ICH. This review discusses the recent advances in pre-clinical and clinical studies on ICH, including the identification of therapeutic targets and ongoing clinical trials. The mechanisms of brain injury following ICH, such as primary and secondary injuries, are also described. Primary injuries include physical disruption of cellular architecture and increased intracranial pressure due to the mass effect of the hematoma. Secondary injuries involve a cascade of events initiated by the primary injury, including inflammation, release of clot components, and disruption of the blood-brain barrier. Therapeutic approaches targeting these mechanisms are being explored, including thrombin inhibition, anti-inflammatory agents, and iron chelation. The role of complement system, free radicals, and other blood components in ICH-induced brain injury is also discussed. The review highlights the importance of understanding the unique mechanisms of ICH-induced brain injury compared to ischemic stroke when designing clinical trials.Intracerebral hemorrhage (ICH) accounts for 10-15% of all strokes and is associated with high mortality and morbidity. Despite significant advances in animal models and understanding of brain injury mechanisms, there is no successful Phase III clinical trial for ICH. This review discusses the recent advances in pre-clinical and clinical studies on ICH, including the identification of therapeutic targets and ongoing clinical trials. The mechanisms of brain injury following ICH, such as primary and secondary injuries, are also described. Primary injuries include physical disruption of cellular architecture and increased intracranial pressure due to the mass effect of the hematoma. Secondary injuries involve a cascade of events initiated by the primary injury, including inflammation, release of clot components, and disruption of the blood-brain barrier. Therapeutic approaches targeting these mechanisms are being explored, including thrombin inhibition, anti-inflammatory agents, and iron chelation. The role of complement system, free radicals, and other blood components in ICH-induced brain injury is also discussed. The review highlights the importance of understanding the unique mechanisms of ICH-induced brain injury compared to ischemic stroke when designing clinical trials.